Background: The preplacodal region (PPR) is a region of specialized ectoderm at the border of neural and nonneural ectoderm (NNE). Coordinated Bmp, Fgf, and Wnt signals are known to drive PPR development; however, the underlying mechanism is unknown. Results: We identified key components involved in PPR differentiation. The mesoderm/marginal Wnts at the early gastrula stage trigger differentiation by allowing the adjacent NNE border cells to start adopting caudal PPR fates; otherwise, the development of caudal PPR identity is hindered due to the persistent presence of gata3 mRNA. The caudal PPR fate dominates when foxi1 expression is enhanced at the late gastrula stage, and depleting Foxi1 after 6 hours postfertilization (hpf) reduces the otic-epibranchial placodal domain. When the Gata3 level is manipulated at the fertilized egg stage or near 6 hpf, the lens is always affected. In establishing PPR polarity, both Gata3 and Foxi1 inhibit Bmp signaling, whereas Foxi1 inhibits, but Gata3 enhances, Fgf sensitivity of the PPR cells. Conclusions: Our study reveals that in zebrafish, (1) the PPR at the shield stage may enter a developmental state when the PPR cells preferentially adopt a particular placodal fate and (2) a network of genetically linked factors, including Wnt/beta-catenin, Fgfr, Bmp, Gata3, and Foxi1, direct the process of PPR differentiation. (C) 2014 Wiley Periodicals, Inc.

Based on a diesel engine fuelled with BD20 biodiesel, particle number (PN) emission characteristics of the engine equipped with DOC, DOC+DPF and none after-treatment device were investigated respectively by engine bench tests. Results showed that both of DOC and DOC+DPF reduced PN emissions, DOC mainly reduced PN in size range of 30nm similar to 50nm smaller diameter, DPF reduced PN of particles larger than 10nm diameter obviously. PN reduction rate of DOC and DOC+DPF were 5%similar to 35% and 60%similar to 98%, DPF contributed 35%similar to 90% of PN reduction rate on the base of DOC. The after-treatment combination of DOC+DPF was recommended as the device with high efficiency in particle number emission control of biodiesel engine.

Highlights • Two novel Streptococcus dysgalactiae GapC CD4+ T-cell epitopes were for the first time identified. • Two epitopes, GapC63–77 and GapC96–110, preferentially elicited polarized Th1 or Th17-type responses. • Our findings are available for further study of epitope-based vaccines. Abstract The GapC protein is highly conserved surface dehydrogenase among Streptococcus dysgalactiae (S. dysgalactiae) and is shown to be involved in bacterial virulence. Immunization of GapC protein can induce specific CD4+ T-cell immune responses and protect against S. dysgalactiae infection. However, there are no studies to identify immunodominant CD4+ T-cell epitopes on GapC protein. In this study, in silico MHC affinity measurement method was firstly used to predict potential CD4+ T-cell epitopes on GapC protein. Six predictive 15-mer peptides were synthesized and two novel GapC CD4+ T-cell epitopes, GapC63–77 and GapC96–110, were for the first time identified using CD4+ T-cells obtained from GapC-immunized BALB/c (H-2d) and C57BL/6 (H-2b) mice spleen based on cell proliferation and cytokines response. The results showed that peptides containing 63–77 and 96–110 induced significant antigen-specific CD4+ T-cells proliferation response in vivo. At the same time, high levels of IFN-γ and IL-17A, as well as moderate levels of IL-10 and IL-4 were detected in CD4+ T-cells isolated from both GapC and peptide-immunized mice in vivo, suggesting that GapC63–77 and GapC96–110 preferentially elicited polarized Th1/Th17-type responses. The characterization of GapC CD4+ T-cell epitopes not only helps us understand its protective immunity, but also contributes to design effective T-cell epitope-based vaccine against S. dysgalactiae infection.